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Signals transduced by inhibitory receptors that recognize self-MHC class I molecules prevent NK cells from being activated by autologous healthy target cells. In order for NK cells to be activated upon contact with an infected cell, the balance between the activating and inhibitory signals that regulate NK cell function must be altered in favor of activation. By studying liver-derived NK cells, we show that only a subpopulation of NK cells expressing high levels of the inhibitory receptor NKG2A are able to lyse autologous vaccinia-infected targets, and that this is due to selective down-regulation of HLA-E. These data demonstrate that release from an inhibitory receptor:ligand interaction is one mechanism that permits NK cell recognition of a virally infected target, and that the variegated expression of inhibitory receptors in humans generates a repertoire of NK cells with different antiviral potentials.

Original publication

DOI

10.4049/jimmunol.176.2.1141

Type

Journal article

Journal

Journal of immunology (Baltimore, Md. : 1950)

Publication Date

01/2006

Volume

176

Pages

1141 - 1147

Addresses

The School of Medicine, Southampton University, Southampton, United Kingdom.

Keywords

Liver, Killer Cells, Natural, Clone Cells, Humans, Vaccinia virus, Receptors, Immunologic, DNA, Histocompatibility Antigens Class I, HLA-A Antigens, HLA-A1 Antigen, HLA Antigens, Ligands, Transfection, Signal Transduction, Cytotoxicity, Immunologic, Down-Regulation, Base Sequence, Receptors, KIR, Immunity, Innate, Receptors, Natural Killer Cell, NK Cell Lectin-Like Receptor Subfamily C, In Vitro Techniques